Abstract
Allergic asthma is a heterogeneous and genetically complex disease that is characterized by the presence of allergen-specific IgE, eosinophilic airway inflammation, and hyperresponsiveness to bronchospasmogenic stimuli. To facilitate the mapping of genes controlling complex asthma traits, we have used a powerful tool, the recombinant congenic strains of mice, which transforms a multigenic difference into a set of monogenic or oligogenic differences.1 This approach offers a higher resolution power than do the standard mouse crosses in mapping segregating quantitative trait loci and in the detection of their potential interactions.
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